Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1995-6-23
pubmed:abstractText
Adhesion of polymorphonuclear leukocytes (PMN) to endothelial cells is an early key event in the inflammatory response and plays an important part in the pathogenesis of septic shock, contributing to vascular and tissue injury. Lipopolysaccharides (LPS) activate endothelial cells to enhanced expression of adhesion molecules. We investigated the interaction of human PMN with resting and LPS-activated human umbilical vein endothelial cells. The activation of endothelial cells by LPS alone did not lead to direct functional or morphological changes as measured by detachment of the endothelial cells from a monolayer and transendothelial albumin flux. LPS induced an increased adhesion of unstimulated PMN to endothelial cells. This was accompanied by endothelial detachment and increased permeability across a monolayer. Endothelial cell lysis as measured by 51Cr release was unaffected. Stimulation of PMN with phorbol ester did not further increase adherence, detachment, or permeability. We conclude that LPS activates endothelial cells and renders cultured monolayers more susceptible to PMN-induced damage. This may provide further insight into the relationship between PMN activation and endothelial damage in Gram-negative sepsis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1073-2322
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
296-300
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Lipopolysaccharide induces hyperadhesion of endothelial cells for neutrophils leading to damage.
pubmed:affiliation
Eijkman-Winkler Institute for Medical Microbiology, University of Utrecht, The Netherlands.
pubmed:publicationType
Journal Article, Comparative Study